Reference - Detail
|Author||Nakano T, Morishita S, Katafuchi A, Matsubara M, Horikawa Y, Terato H, Salem AM, Izumi S, Pack SP, Makino K, Ide H.|
|Title||Nucleotide excision repair and homologous recombination systems commit differentially to the repair of DNA-protein crosslinks.|
DNA-protein crosslinks (DPCs)-where proteins are covalently trapped on the DNA strand-block the progression of replication and transcription machineries and hence hamper the faithful transfer of genetic information. However, the repair mechanism of DPCs remains largely elusive. Here we have analyzed the roles of nucleotide excision repair (NER) and homologous recombination (HR) in the repair of DPCs both in vitro and in vivo using a bacterial system. Several lines of biochemical and genetic evidence show that both NER and HR commit to the repair or tolerance of DPCs, but differentially. NER repairs DPCs with crosslinked proteins of sizes less than 12-14 kDa, whereas oversized DPCs are processed exclusively by RecBCD-dependent HR. These results highlight how NER and HR are coordinated when cells need to deal with unusually bulky DNA lesions such as DPCs.
|MeSH||Animals Azacitidine / metabolism Chromosomes / genetics Cross-Linking Reagents / metabolism DNA / genetics DNA / metabolism* DNA Damage* DNA Helicases / genetics DNA Helicases / metabolism DNA Repair* DNA Replication* Endodeoxyribonucleases / metabolism Escherichia coli / metabolism Escherichia coli Proteins / genetics Escherichia coli Proteins / metabolism Exodeoxyribonuclease V / genetics Exodeoxyribonuclease V / metabolism Formaldehyde / metabolism Humans Plasmids / genetics Plasmids / metabolism Recombination, Genetic*|
|WOS Category||BIOCHEMISTRY & MOLECULAR BIOLOGY CELL BIOLOGY|
|Prokaryotes E. coli||ME8083 ME8680(E486)|